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TGFBR2-dependent alterations of exosomal cargo and functions in DNA mismatch repair-deficient HCT116 colorectal cancer cells

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Colorectal cancers (CRCs) that lack DNA mismatch repair function exhibit the microsatellite unstable (MSI) phenotype and are characterized by the accumulation of frameshift mutations at short repetitive DNA sequences (microsatellites). These tumors recurrently show inactivating frameshift mutations...

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Main Authors: Fricke, Fabia (Author) , Lee, Jennifer (Author) , Michalak, Malwina (Author) , Haußer-Siller, Ingrid (Author) , Suarez-Carmona, Meggy (Author) , Halama, Niels (Author) , Kopitz, Jürgen (Author) , Gebert, Johannes (Author)
Format: Article (Journal)
Language:English
Published: 4 April 2017
In: Cell communication and signaling
Year: 2017, Volume: 15
ISSN:1478-811X
DOI:10.1186/s12964-017-0169-y
Online Access:Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1186/s12964-017-0169-y
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Author Notes:Fabia Fricke, Jennifer Lee, Malwina Michalak, Uwe Warnken, Ingrid Hausser, Meggy Suarez-Carmona, Niels Halama, Martina Schnölzer, Jürgen Kopitz and Johannes Gebert
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Summary:Colorectal cancers (CRCs) that lack DNA mismatch repair function exhibit the microsatellite unstable (MSI) phenotype and are characterized by the accumulation of frameshift mutations at short repetitive DNA sequences (microsatellites). These tumors recurrently show inactivating frameshift mutations in the tumor suppressor Transforming Growth Factor Beta Receptor Type 2 (TGFBR2) thereby abrogating downstream signaling. How altered TGFBR2 signaling affects exosome-mediated communication between MSI tumor cells and their environment has not been resolved. Here, we report on molecular alterations of exosomes shed by MSI cells and the biological response evoked in recipient cells.
Item Description:Gesehen am 04.05.2017
Physical Description:Online Resource
ISSN:1478-811X
DOI:10.1186/s12964-017-0169-y

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